Transcript Rheumatic Fever

RHEUMATIC
FEVER &
RHEUMATIC
HEART DISEASE
Dr Sarika Gupta (MD,PhD); Asst. Professor
ACUTE RHEUMATIC FEVER
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Autoimmune consequence of infection (pharyngeal
infection not the skin infection) with Group A beta
haemolytic streptococcal infection
Generalized inflammatory response affecting brains,
joints, skin, subcutaneous tissues & the heart
Modified Duckett-Jones criteria form the basis of
the diagnosis of the condition
ACUTE RHEUMATIC FEVER
Supporting evidences:
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About 66% of the patients with an acute episode of
rheumatic fever have a history of an upper
respiratory tract infection several weeks before
The peak age (6-15 yrs) & seasonal incidence of acute
rheumatic fever closely parallel those of GABHS
infections
ACUTE RHEUMATIC FEVER
Features suggestive of GABHS infection
 Patient 5 to 15 years of age
 Presentation in winter or early spring
 Fever, Headache
 Sudden onset of sore throat
 Nausea, vomiting & abdominal pain; Pain with
swallowing
 Beefy, swollen, red uvula
 Soft palate petechiae (“doughnut lesions”)
 Tender, enlarged anterior cervical nodes
 Tonsillopharyngeal erythema & exudates
ACUTE RHEUMATIC FEVER
Redness & swelling
of throat & tonsils;
Beefy, swollen, red
uvula; Soft palate
petechiae
(“doughnut
lesions”)
Sore throat: fever,
white draining
patches on the
throat & swollen or
tender lymph glands
in the neck
Tonsillopharyngeal
erythema &
exudates
ACUTE RHEUMATIC FEVER
Supporting evidences:
 Patients with acute rheumatic fever almost always
have serologic evidence of a recent GABHS infection
 Their antibody titers are usually considerably higher
than those in patients with GABHS infections without
acute rheumatic fever
 Antimicrobial therapy against GABHS: prevents initial
episodes of acute rheumatic fever &
 Long-term, continuous prophylaxis: prevents
recurrences of acute rheumatic fever
ACUTE RHEUMATIC FEVER
Predisposing factors:
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Family history of rheumatic fever
Low socioeconomic status (poverty, poor hygiene,
medical deprivation)
Age: 6-15 years
EPIDEMIOLOGY
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Prevalence of Acute rheumatic fever & RHD:
0.67/1000 to 11/1000 children
The INCIDENCE of rheumatic fever varies from
0.2 to 0.75/1000/ year in schoolchildren 5–15 years
of age (2001 Govt. Census)
certain M proteins
(M1, M5, M6, and
M19) share
epitopes with
human
tropomyosin &
myosin
Common antigenic determinants are
shared between components of GAS
(M protein, protoplast membrane,
cell wall group A carbohydrate,
capsular hyaluronate) & specific
mammalian tissues (e.g., heart, brain,
joint)
strong correlation between progression
to RHD & HLA-DR class II alleles &
the inflammatory protein-encoding genes
MBL2 and TNFA
Pathogenetic pathway for ARF & RHD
CLINICAL MANIFESTATIONS
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No pathognomonic clinical or laboratory finding for
acute rheumatic fever
Duckett Jones in 1944 proposed guidelines to aid in
diagnosis & to limit overdiagnosis
Jones criteria for the diagnosis of acute rheumatic
fever 2 major criteria or 1 major & 2 minor
criteria along with the absolute requirement
There are 5 major and 4 minor criteria & an
absolute requirement for evidence (microbiologic or
serologic) of recent GABHS infection
DIAGNOSIS
MAJOR
MANIFESTATIONS
MINOR
MANIFESTATIONS
Carditis
Clinical features:
Arthralgia
Fever
SUPPORTING EVIDENCE OF
ANTECEDENT GROUP A
STREPTOCOCCAL
INFECTION******
-Elevated or increasing
streptococcal antibody titer
Polyarthritis
Erythema
marginatum
Subcutaneous
nodules
Chorea
Laboratory features:
Elevated acute phase
reactants: ESR, C-reactive
protein
Prolonged PR interval
History of (<45 days)
-Positive throat culture or rapid
streptococcal antigen test or
streptococcal sore throat or
scarlet fever)
ARF & RHD
First episode
or Recurrence
without
established
heart
disease: 2
major
criteria or 1
major & 2
minor criteria
& the
absolute
requirement
Recurrence
with
established
heart
disease: 2
minor criteria
and the
absolute
requirement
MAJOR
MANIFESTATIONS
Migratory Polyarthritis
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Most common (75%)
Involves larger joints: the knees, ankles, wrists &
elbows
Rheumatic joints: hot, red, swollen & exquisitely
tender (friction of bedclothes is uncomfortable)
The pain can precede & can appear to be
disproportionate to the other findings
Migratory Polyarthritis
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The joint involvement is characteristically migratory
in nature
Monoarticular arthritis is unusual unless anti
inflammatory therapy is initiated prematurely,
aborting the progression of the migratory
polyarthritis
Migratory Polyarthritis
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If a child with fever and arthritis is suspected of
having acute rheumatic fever: withhold salicylates &
observe for migratory progression
A dramatic response to even small doses of
salicylates is another characteristic feature of the
arthritis
Rheumatic arthritis is typically not deforming
Migratory Polyarthritis
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Arthritis; earliest manifestation of acute rheumatic
fever
Correlate temporally with peak antistreptococcal
antibody titers
An inverse relationship between the severity of
arthritis & the severity of cardiac involvement
Carditis
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Carditis & chronic rheumatic heart disease: most
serious manifestations of acute rheumatic fever
Account for essentially all of the associated
morbidity and mortality
Occurs in 50% of patients
Rheumatic carditis: pancarditis with active
inflammation of myocardium, pericardium &
endocardium
Acute rheumatic carditis: tachycardia out of
proportion to fever & cardiac murmurs, with or
without evidence of myocardial or pericardial
involvement
Carditis
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Consists of either isolated mitral valvular disease or
combined aortic & mitral valvular disease
Valvular insufficiency: characteristic of both acute &
convalescent stages of acute rheumatic fever
Mitral regurgitation: a high-pitched apical
holosystolic murmur radiating to the axilla
In patients with significant mitral regurgitationassociated with an apical mid-diastolic murmur of
relative mitral stenosis
Aortic insufficiency: a high-pitched decrescendo
diastolic murmur at the upper left sternal border
Carditis
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Valvular stenosis: appears several years or even
decades after the acute illness
However, in developing countries where acute
rheumatic fever often occurs at a earlier age, mitral
stenosis & aortic stenosis may develop in young
children
Moderate to severe rheumatic carditis:
cardiomegaly & congestive heart failure with
hepatomegaly & peripheral & pulmonary edema
Myocarditis &/or pericarditis without evidence of
endocarditis: rarely due to rheumatic heart disease
Carditis
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Echocardiographic findings: pericardial effusion,
decreased ventricular contractility & aortic &/or
mitral regurgitation
The major consequence of acute rheumatic carditis
is chronic, progressive valvular disease
During an episode of
ARF, valve changes can
be minor and are still
able to regress
After recurrent
episodes of ARF,
thickening of subvalvar
apparatus, chordal
thickening and
shortening and
progression to
permanent valve damage
is evident
Chorea
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St. Vitus’dance
Sydenham chorea: 10-15% of patients with acute
rheumatic fever
Often in prepubertal girls (8-12 yrs)
A long latency period (1-6 mo) between
streptococcal pharyngitis & the onset of chorea
Neuropsychiatric disorder
Neurologic signs: choreic movement & hypotonia
Psychiatric signs: emotional lability, hyperactivity,
separation anxiety, obsessions & compulsions
Chorea
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Begins with emotional lability & personality changes
(poor school performance)
Replace in 1-4 weeks by characteristic spontaneous,
purposeless movement of chorea (lasts 4-8 months)
followed by motor weakness
Exacerbation by stress & disappearing with sleep
are characteristic
Elevated titers of “antineuronal antibodies” against
basal ganglion tissues have been found in over 90%
of patients
Chorea
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Clinical maneuvers to elicit features of chorea
include
(1) demonstration of milkmaid's grip (irregular
contractions of the muscles of the hands while
squeezing the examiner's fingers)
(2) spooning and pronation of the hands when the
patient's arms are extended
(3) wormian darting movements of the tongue upon
protrusion
(4) examination of handwriting to evaluate fine motor
movements
Chorea
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Diagnosis: based on clinical findings with supportive
evidence of GABHS antibodies
In patients with a long latent period: antibody levels
may have declined to normal
SUBCLINICAL CARDITIS-30%
Although the acute illness is distressing, chorea
rarely, if ever, leads to permanent neurologic
sequelae
Erythema Marginatum
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A rare (<3% of patients with acute rheumatic fever)
but characteristic rash of acute rheumatic fever
It consists of erythematous,
serpiginous, macular lesions with
pale centers that are not pruritic
It occurs primarily on the trunk
& extremities, not on the face &
it can be accentuated by warming
the skin
Subcutaneous Nodules
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A rare (≤1% of patients with acute rheumatic fever)
finding
Consist of firm nodules approximately 1 cm in
diameter along the extensor surfaces of tendons
near bony prominences
A correlation between the presence of these
nodules & significant
rheumatic heart disease
MINOR
MANIFESTATIONS
MINOR MANIFESTATIONS
Clinical:
 1. Arthralgia (in the absence of polyarthritis as a
major criterion)
 2. Fever (typically temperature ≥102°F & occurring
early in the course of illness)
Laboratory minor manifestations:
 1.Elevated acute-phase reactants (C-reactive protein,
erythrocyte sedimentation rate, polymorphonuclear
leukocytosis)
 2. Prolonged PR interval on electrocardiogram (1st
degree heart block)
ESSENTIAL CRITERIA
An absolute requirement for the
diagnosis of acute rheumatic fever is
supporting evidence of a recent GABHS
infection
Recent Group A Streptococcus infection
Hallmarks of GAS sore throat:
 High fever, tender anterior cervical lymph nodes
 Close contact with infected person
 Strawberry tongue, petechiae on palate
 Excoriated nares( crusted lesions) in infants
 Tonsillar exudates in older children
 Abdominal pain
GOLD STANDARD: POSITIVE THROAT CULTURE

Recent Group A Streptococcus infection
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Acute rheumatic fever typically develops 2-4 wk
after an acute episode of GABHS pharyngitis at a
time when clinical findings of pharyngitis are no
longer present & only 10-20% of the throat culture
or rapid streptococcal antigen test results are
positive
Therefore, evidence of an antecedent GABHS
infection is usually based on elevated or increasing
serum antistreptococcal antibody titers
Recent Group A Streptococcus infection
1. ASO titre:
 well standardized
 elevated in 80% of patients with ARF
 ASO titre of 333 Todd unit in children & 250 Todd
unit in adults are considered elevated
2. Antideoxyribonuclease B titre:
 ≥240 Todd unit in children & ≥120 Todd unit in adults
Recent Group A Streptococcus infection
3. Slide agglutination test (Streptozyme):
 Detect antibodies against 5 different GABHS
antigens
 Rapidly, relatively simple to perform & widely
available
 Less standardized & less reproducible than other
tests and should not be used as a diagnostic test for
evidence of an antecedent GAS infection
Recent Group A Streptococcus infection
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Single antibody measured: 80-85% of patients have
an elevated titer
If 3 different antibodies (antistreptolysin O, antiDNase B, antihyaluronidase) measured: 95-100% have
an elevation
Therefore in suspectedARF clinically: perform
multiple antibody tests
Diagnosis of ARF should not be made in patients with
elevated or increasing streptococcal antibody titers
who do not fulfill the Jones criteria
True for younger, school-aged children having
GABHS pyoderma or GABHS pharyngitis
DIFFERENTIAL DIAGNOSIS
ARTHRITIS
Rheumatoid arthritis
Reactive arthritis (Shigella, Salmonella, Yersinia)
Serum sickness
Sickle cell disease
Malignancy
Systemic lupus erythematosus
Lyme disease (Borrelia burgdorferi)
Gonococcal infection (N.gnorrhoeae)
DIFFERENTIAL DIAGNOSIS
CARDITIS
Viral myocarditis
Viral pericarditis
Infective endocarditis
Kawasaki disease
Congenital heart disease
Mitral valve prolapse
Innocent murmurs
DIFFERENTIAL DIAGNOSIS
CHOREA
Huntington chorea
Wilson disease
Systemic lupus erythematosus
Cerebral palsy
Tics
Hyperactivity
DIFFERENTIAL DIAGNOSIS
Patients with infective endocarditis: present with
both joint and cardiac manifestations
These patients can usually be distinguished from
patients with acute rheumatic fever by blood
cultures & the presence of associated findings
(hematuria, splenomegaly, splinter hemorrhages)
TREATMENT
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Bed rest
Antibiotic Therapy:
10 days of orally administered penicillin or
erythromycin or a single intramuscular injection of
benzathine penicillin to eradicate GABHS from the
upper respiratory tract
Afterwards, the patient should be started on longterm antibiotic prophylaxis
TREATMENT
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Anti-inflammatory Therapy:
Anti-inflammatory agents (salicylates,
corticosteroids) should be withheld if arthralgia or
atypical arthritis is the only clinical manifestation of
presumed acute rheumatic fever
Acetaminophen can be used
Patients with typical migratory polyarthritis & with
carditis without cardiomegaly or congestive heart
failure:
treatment with oral salicylates, 100 mg/kg/day in 4
divided doses PO for 3-5 days, followed by
75 mg/kg/day in 4 divided doses PO for 4-8 wk
TREATMENT
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Patients with carditis & cardiomegaly or congestive
heart failure:
treatment with corticosteroids
Prednisone 2 mg/kg/day in 4 divided doses for 2-6 wk
followed by a tapering of the dose that reduces the
dose by 5 mg/24 hr every 2-3 days. At the beginning
of the tapering of the prednisone dose, aspirin should
be started at 75 mg/kg/day in 4 divided doses to
complete 12 wk of therapy
TREATMENT
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Supportive therapies for patients with moderate to
severe carditis include digoxin, fluid & salt
restriction, diuretics & oxygen
The cardiac toxicity of digoxin is enhanced with
myocarditis
TREATMENT
Sydenham Chorea
 Occurs after the resolution of the acute phase of
the disease
 Anti-inflammatory agents are usually not indicated
 Sedatives: phenobarbital (16-32 mg every 6-8 hr PO)
is the drug of choice
 If phenobarbital is ineffective, then haloperidol
(0.01-0.03 mg/kg/24 hr divided bid PO) or
chlorpromazine (0.5 mg/kg every 4-6 hr PO) should
be initiated
 Long-term antibiotic prophylaxis
PREVENTION
PREVENTION
PRIMARY-10 days course
of penicillin therapy;
about 30% of patients with
acute rheumatic fever do
not recall a preceding
episode of pharyngitis
SECONDARY-Secondary
prevention is directed at
preventing acute GABHS
pharyngitis in patients at
substantial risk of
recurrent acute rheumatic
fever
SECONDARY PREVENTION
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Who should receive prophylaxis?
Patients with documented history of rheumatic fever,
including those with isolated chorea & those without
evidence of rheumatic heart disease MUST receive
prophylaxis
SECONDARY PREVENTION
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For how long?
CATEGORY
Rheumatic fever without carditis
DURATION
At least for 5 yr or until
age 21 year, whichever is
longer
Rheumatic fever with carditis but At least for 10 yr or well
without residual heart disease (no into adulthood, whichever is
valvular disease)
longer
Rheumatic fever with carditis &
residual heart disease (persistent
valvular disease)
At least 10 yr since last
episode & at least until age
40 yr; sometime lifelong
SECONDARY PREVENTION
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What method of prophylaxis should be used?
DRUG
Penicillin G benzathine
DOSE
ROUTE
600,000 U for children, ≤27 kg
1.2 million U for children >27 kg, Intramuscular
every 3 wk
OR
Penicillin V
250 mg, twice a day
OR
Oral
0.5 g, once a day for patients
≤60 lb; 1.0 g, once a day for
Oral
patients >60 lb
For people who are allergic to penicillin and sulfonamide drugs
Sulfadiazine or
sulfisoxazole
Macrolide or azalide
Variable
Oral
RHEUMATIC HEART DISEASE
Rheumatic involvement of the valves & endocardium
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The valvular lesions begin as small verrucae composed of fibrin and
blood cells along the borders of one or more of the heart valves
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The mitral valve is affected most often, followed in frequency by
the aortic valve; right-sided heart manifestations are rare
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At the end of inflammation: verrucae disappear & leave scar tissue
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Repeated attacks of rheumatic fever: new verrucae form near the
previous ones & the mural endocardium & chordae tendineae become
involved
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MITRAL INSUFFICIENCY
Backflow of blood from the LV to the LA during
systole
MITRAL INSUFFICIENCY
Pathophysiology:
 Loss of valvular substance & shortening &
thickening of the chordae tendineae
 Because of the high volume load & inflammatory
process, the left ventricle becomes enlarged
 The left atrium dilates as blood regurgitates into
this chamber
 Increased left atrial pressure results in pulmonary
congestion & symptoms of left-sided heart failure
MITRAL INSUFFICIENCY
Clinical manifestations:
 Exertion Dyspnea ( exercise intolerance), fatigue
 Mild disease : NO signs of heart failure
 Severe mitral insufficiency: signs of left sided heart
failure
 The heart is enlarged, with a forcible & hyperkinetic
apical left ventricular impulse & often an apical
systolic thrill
 Soft S1
MITRAL INSUFFICIENCY
Clinical manifestations:
 The 2nd heart sound may be accentuated if
pulmonary hypertension is present
 A 3rd heart sound is generally prominent
 A holosystolic murmur is heard at the apex with
radiation to the axilla
 A short mid-diastolic rumbling murmur is caused by
increased blood flow across the mitral valve as a
result of the insufficiency
MITRAL INSUFFICIENCY
Imaging studies:
 ECG: prominent bifid P waves, signs of left
ventricular hypertrophy & associated right
ventricular hypertrophy if pulmonary hypertension is
present
 X-rays: prominence of the left atrium & ventricle;
congestion of perihilar vessels, a sign of pulmonary
venous hypertension
 2 D ECHO: enlargement of the left atrium & ventricle
& Doppler studies demonstrate the severity of the
mitral regurgitation
MITRAL INSUFFICIENCY
Complications:
 cardiac failure
 chronic mitral insufficiency -right ventricular failure
 atrial and ventricular arrhythmias
MITRAL INSUFFICIENCY
Management:
 Medical:
 Prophylaxis against recurrences of rheumatic fever
 Treatment of heart failure, arrhythmias and
infective endocarditis
 Afterload-reducing agents (ACE inhibitors or
angiotensin receptor blockers):
reduce the regurgitant volume & preserve left
ventricular function
MITRAL INSUFFICIENCY
Management:
 Surgical:
 For patients who despite adequate medical therapy
have persistent heart failure, dyspnea with moderate
activity & progressive cardiomegaly, often with
pulmonary hypertension
 Valve repair surgery preferred over valve replacement
MITRAL STENOSIS
Obstruction of LV inflow that prevents proper
filling during diastole
2
Normal MV Area: 4-6 cm
Transmitral gradients & symptoms begin at
areas less than 2 cm2

MITRAL STENOSIS
Pathophysiology:
 From fibrosis of the mitral ring, commissural
adhesions & contracture of the valve leaflets, chordae
& papillary muscles
 It takes 10 years or more for the lesion to become
fully established
MITRAL STENOSIS
Pathophysiology:
 Significant mitral stenosis results in increased
pressure, enlargement & hypertrophy of the left
atrium, pulmonary venous hypertension, increased
pulmonary vascular resistance & pulmonary
hypertension
 Right ventricular hypertrophy & right atrial
dilatation ensue & are followed by right ventricular
dilation, tricuspid regurgitation & clinical signs of
right-sided heart failure
MITRAL STENOSIS
Clinical manifestations:
 Correlation between symptoms & the severity of
obstruction
 Patients with mild lesions: asymptomatic
 More severe degrees of obstruction: exercise
intolerance & dyspnea
 Critical lesions: orthopnea, paroxysmal nocturnal
dyspnea, & overt pulmonary edema, as well as atrial
arrhythmias
MITRAL STENOSIS
Clinical manifestations:
 Pulmonary hypertension: right ventricular dilatationfunctional tricuspid insufficiency, hepatomegaly,
ascites & edema
 Hemoptysis: rupture of bronchial or pleurohilar veins
or by pulmonary infarction
MITRAL STENOSIS
Clinical manifestations:
 Jugular venous pressure is increased in severe
disease with heart failure
 prominent "a" wave in jugular venous pulsations: Due
to pulmonary hypertension & right ventricular
hypertrophy
 Mild disease: heart size is normal, tapping apex
 Severe mitral stenosis: moderate cardiomegaly
 Cardiac enlargement massive: atrial fibrillation &
heart failure
 A parasternal right ventricular lift is palpable when
pulmonary pressure is high
MITRAL STENOSIS
Clinical manifestations:
 Auscultatory findings:
 Loud 1st heart sound,
 An opening snap of the mitral valve, and
 A long, low-pitched, rumbling mitral diastolic murmur
with presystolic accentuation at the apex
 Murmur absent in patients with significant heart
failure
MITRAL STENOSIS
Clinical manifestations:
 A holosystolic murmur secondary to tricuspid
insufficiency
 Pulmonary hypertension: pulmonic component of the
2nd heart sound is accentuated
 An early diastolic murmur: associated AR or pulmonary
valvular insufficiency secondary to pulmonary
hypertension
MITRAL STENOSIS
Imaging studies:
 ECG: prominent & notched P waves & varying degrees
of right ventricular hypertrophy, Atrial fibrillation
 X-rays: Left atrial enlargement & prominence of the
pulmonary artery & right-sided heart chambers;
calcifications may be noted in the region of the
mitral valve
 Severe obstruction is associated with a
redistribution of pulmonary blood flow so that the
apices of the lung have greater perfusion (the
reverse of normal)
MITRAL STENOSIS
Imaging studies:
 2 D ECHO: thickening of the mitral valve, distinct
narrowing of the mitral orifice during diastole and
left atrial enlargement
 Doppler can estimate the transmitral pressure
gradient
 Cardiac catheterization quantitates
 Diastolic gradient across the mitral valve
 Allows for the calculation of valve area
 Assesses the degree of elevation of pulmonary
arterial pressure
MITRAL STENOSIS
Management:
 Medical:
 Mild & moderate MS: anticongestive measures
(digoxin & diuretics)
 Atrial fibrillation: digoxin; procainamide for
conversion to sinus rhythm in hemodynamiclly stable
patients
 chronic AF warfarin
 IE prophylaxis
 percutaneous mitral balloon valvotomy: failure to
thrive with repeated respiratory infections
MITRAL STENOSIS
Management:
 Surgical: indicated in
 patients with clinical signs & hemodynamic evidence of
severe obstruction
 or ANY SYMPTOMATIC Patient with NYHA Class III
or IV Symptoms
 or Asymptomatic moderate or severe MS with a
pliable valve
MITRAL STENOSIS
Management:
 Surgical valvotomy or balloon catheter mitral
valvuloplasty
 Balloon valvuloplasty is indicated for symptomatic,
stenotic, pliable, noncalcified valves of patients
without atrial arrhythmias or thrombi
AORTIC INSUFFICIENCY
Leakage of blood into LV during diastole due to
ineffective coaptation of the aortic cusps
Regurgitation of blood leads to volume overload
with dilatation & hypertrophy of the left
ventricle
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AORTIC INSUFFICIENCY
Pathophysiology:
 Combined pressure AND volume overload
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Compensatory Mechanisms: LV dilation & LV
hypertrophy
Progressive dilation leads to heart failure
AORTIC INSUFFICIENCY
Clinical manifestations:
 Symptoms are unusual except in severe aortic
insufficiency
 The large stroke volume & forceful left ventricular
contractions result in palpitations
 Sweating and heat intolerance are related to
excessive vasodilation
 Dyspnea on exertion can progress to orthopnea and
pulmonary edema
 Nocturnal attacks with sweating, tachycardia, chest
pain, & hypertension
AORTIC INSUFFICIENCY
Clinical manifestations:
 Wide pulse pressure with bounding peripheral pulses
 Systolic blood pressure elevated & diastolic pressure
is lowered
 Severe aortic insufficiency: enlarged heart with a
left ventricular apical heave
 Diastolic thrill unusual
 Murmur begins immediately with the 2nd heart sound
& continues until late in diastole over the upper &
midleft sternal border with radiation to the apex and
upper right sternal border
AORTIC INSUFFICIENCY
Clinical manifestations:
 It has a high-pitched blowing quality & is easily
audible in full expiration with the diaphragm of the
stethoscope placed firmly on the chest & the patient
leaning forward
 An aortic systolic ejection murmur is frequent
because of the increased stroke volume
 An apical presystolic murmur (Austin Flint
murmur) resembling MS is sometimes heard (due to
the large regurgitant aortic flow in diastole
preventing the mitral valve from opening fully)
Auscultatory and peripheral findings
in severe AR
AORTIC INSUFFICIENCY
Imaging studies:
 ECG: signs of left ventricular hypertrophy & strain
with prominent P waves in severe cases
 X-rays: Enlargement of the left ventricle & aorta
AORTIC INSUFFICIENCY
Imaging studies:
 2 D ECHO:
 A large left ventricle & diastolic mitral valve flutter
or oscillation caused by regurgitant flow hitting the
valve leaflets
 Doppler studies demonstrate the degree of aortic
runoff into the left ventricle
 Magnetic resonance angiography can be useful in
quantitating regurgitant volume
 Cardiac catheterization is necessary only when the
echocardiographic data are equivocal
AORTIC INSUFFICIENCY
Management:
 Mild and moderate lesions are well tolerated. Unlike
mitral insufficiency, aortic insufficiency does not
regress
 Medical:
 Afterload reducers (ACE inhibitors or angiotensin
receptor blockers)
 Prophylaxis against recurrence of acute rheumatic
fever
 IE prophylaxis
AORTIC INSUFFICIENCY
Management:
 Surgical: Definitive Treatment
 Surgical intervention (valve replacement) should be
carried out well in advance of the onset of heart
failure, pulmonary edema, or angina, when signs of
decreasing myocardial performance become evident
as manifested by increasing left ventricular
dimensions on the echocardiogram
AORTIC INSUFFICIENCY
Management:
 Surgery is considered when early symptoms are
present, ST-T wave changes are seen on the
electrocardiogram, or evidence of decreasing left
ventricular ejection fraction is noted
 ANY Symptoms at rest
 Asymptomatic treatment if: EF drops below 50% or
LV becomes dilated
TRICUSPID VALVE DISEASE





Primary tricuspid involvement : rare
Tricuspid insufficiency: secondary to right
ventricular dilatation resulting from unrepaired leftsided lesions
Signs: prominent pulsations of the jugular veins,
systolic pulsations of the liver & a blowing
holosystolic murmur at the lower left sternal border
that increases in intensity during inspiration
Signs of tricuspid insufficiency decrease or
disappear when heart failure produced by the leftsided lesions is successfully treated
Tricuspid valvuloplasty may be required in rare cases
PULMONARY VALVE DISEASE



Pulmonary insufficiency usually occurs on a functional
basis secondary to pulmonary hypertension & is a late
finding with severe mitral stenosis
The murmur (Graham Steell murmur) is similar to
that of aortic insufficiency, but peripheral arterial
signs (bounding pulses) are absent
The correct diagnosis is confirmed by twodimensional echocardiography and Doppler studies
SUMMARY



Rheumatic heart disease is the
only truly preventable chronic
heart condition
Primary prevention:
Penicillin for suspected strep sore
throat
Secondary prevention
Penicillin prophylaxis